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Resumen de Análisis de polimorfismos de genes asociados al síndrome metabólico en niños obesos

Josune Olza

  • Childhood obesity is currently a major public health problem, resulting in increased morbidity and mortality, while representing a high economic burden on healthcare systems. The prevalence of obesity has increased at an alarming rate. The problem is global and is steadily affecting not only developed countries but also many low- and middle-income countries, particularly in urban areas. Globally, in 2010 the number of overweight children under the age of five was estimated to be over 42 million. Close to 35 million of these are living in developing countries (WHO, 2011).

    Childhood obesity is characterized by low-grade inflammation that leads to numerous co-morbidities such as hypertension, insulin resistance, dyslipidemia, diabetes mellitus type 2, steatosis, orthopaedic problems and sleep apnoea, among others, that may appear in the short or long term. Several studies have demonstrated an association between childhood obesity and the risk of cardiovascular disease (CVD) in adulthood (Freedman et al. 2004), as well as changes in body mass index over time and the prediction of increased concentrations of lipids and lipoproteins in adulthood (Lauer et al. 1988).

    The association of hypertension, hypertriglyceridemia, low (high-density lipoprotein) HDL cholesterol, and impaired glucose metabolism that tend to cluster in obese subjects is termed metabolic syndrome (MS). Insulin resistance appears to be the key in the development of MS, which in turn is strongly associated with the risk of cardiovascular disease and type 2 diabetes mellitus. The prevalence of MS in children has also increased in recent decades, reaching levels of up to 40 percent in some countries (Tailor et al. 2009).

    Besides defined as an imbalance between caloric intake and expenditure, it is known that childhood obesity is related to a number of genetic alterations. According to the characteristics of these alterations it may be monogenic obesity due to the alteration of a specific gene, syndromic obesity represented by clearly identified and recognized entities, namely chromosomic alterations as the case of Prader-Willi syndrome, and polygenic obesity because of single nucleotide polymorphisms (SNPs) and other structural genetic variants affecting various genes.

    In recent years through the human genome wide association studies (GWAS) several gene variants associated with many complex diseases, as in the case of obesity, have been identified. Within that context some causal alleles have been reported; however, most of them confer a moderate risk as they explain a very low proportion of the aetiology of those diseases. There is strong evidence that rare variants play an important role in the aetiology of complex diseases and can have major effects than common genetic variants. This has exposed a major limitation of the GWAS, because they have left out a large number of rare variants, and has created the need to seek other alternatives for consideration such as the selection of candidate genes with differential expression, sequencing of the specific regions of each gene or possibly the entire genome, the use of high-resolution GWAS, which include gene variants with allele frequencies below 5 percent or the use of case-control studies applying new technologies. These and other developments open the door to a new generation of genomic studies in the coming years that will bring new insights into the origin of many diseases.

    With this background, the aim of the present research was to find potential associations between selected SNPs for a number of genes that had been previously demonstrated to be differentially expressed in omental adipose tissue for obese children, as well as other candidate genes, with childhood obesity and the MS and its phenotypes.


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